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CR - Pul Path (i) Bronchiectasis (Presentations (lower lobes most commonly…
CR - Pul Path (i) Bronchiectasis
abnormal irreversible dilatation of bronchioles
due to destruction of muscle + elastic tissue
obstructive (as opposed to restrictive which is caused by parenchymal fibrosis)
Viscous circle
transmural infection
inflamm
mediator release (elastases, trypsin, ROS by neutrophils)
damage + dilation of walls
promotes further pathogen colonisation
prognosis depends on underlying cause + extent of lung involved
Causes
in upper lobe - chronic cavities
CF
TB
in central lobe
CF
ABPA (allergic bronchopul aspergillosis - common in asthmatics + immunosuppressed)
congenital tracheobronchomegaly (abnormally wide)
in lower lobe
sequel of childhood infection
bronchopneumonia
pneumonia complicating measles/pertussis
hence vaccines NB
bronchiolitis
primary MAI complex infection
aspirations
immunodeficiency
hypogammaglobulinaemia (low IgG/M/A - prevented by Ig replacement) or seoncondary to malignancies
congenital
primary ciliary dyskinesia aka Kartagener syndrome
poor functioning cilia
recurrent infections
triad of sinusitis, sinus inversus (major organs are reversed/mirrored from their normal positions) + bronchiectasis)
alpha1AT deficiency
Young's syndrome
bronchiectasis
rhino sinusitis
reduced fertility
Marfan syndrome
obstruction of central bronchi
foreign bodies
tumour
asthmatic mucus
pus
compressive lymphadenopathy
rheumatic conditions
SLE
RA
Sjogrens
IBD (esp ulcerative colitis)
COPD = causative major confounding disease
Presentations
lower lobes most commonly affected
left more than right lung (left bronchus more horizontal - discharge of secretions is slower), but often bilat
productive cough
mucopurulent, mucoid, thick, visors sputum sometimes streaked with blood (ulcerated airway)
copious haemoptysis may result from erosive damage in acute infection
dyspnoea
wheeze
pleuritic pain in 50%
recurrent LRTIs
chronic inflamm + lymphoid follicles in wall
bronchial arts increase in size
crackles/course creps/rhonchi
clubbing (common in past, in only 3% now)
pathogenesis
induced by 2 factors: infectious insult + impairment of drainage/clearance of secretions (obstruction)
bronchi inflamed, dilated, easily collapsable
Histologic changes
cart destruction + fibrosis
mucosal + mucus gland (goblet cell) hyperplasia
inflamm cell infiltration
increased mucus + exudate
loss of cilia
complications
massive haemoptysis
amyloidosis
brain abscess
resp failure
investigations
blood
FBC
U+E
autoIg screen
serum Ig
IgE levels
alpha1AT level
CF sweat tests
micro
sputum culture + stain
blood cultures
look for TB
CXR
CT-thorax (small airways visible as filled with mucus)
bronchoscopy
look for obstruction
washings for culture + cytology
PFTs
Pathological Classification
varicose (string of beads)
cylindrical (tram track)
cystic (cluster of grapes)
not clinically relevant - doesn't impact prognosis or tx
Management
confirm correct underlying Dx
Tx infective exacerbations with nebulised antibiotics
reduce risk factors
possible maintenance antibiotics
influenza + pneumococcal vaccines
chest physiotx
nebulised DNase
WBCs release DNA when they dies - adds to viscosity of mucus
makes mucus easier to clear from lungs
if focal surgical excision